Mycobacterium avium complex, or MAC, includes three species; Mycobacterium avium, Mycobacterium Chimaera, and Mycobacterium intracellulare.
MAC is the most common nontuberculous mycobacteria, or NTM.
The three different species of MAC are difficult to differentiate and cause the same spectrum of diseases, so they are often grouped together.
MAC is very different from Mycobacterium tuberculosis.
MAC lung infection is a chronic disease, often present for several years prior to diagnosis.
It typically has a more indolent course, and can be difficult to eradicate, with frequent recurrences after completing long courses of treatment.
In addition, in immunocompromised individuals, MAC can become disseminated, affecting organs other than the lungs, and can cause lymphadenitis.
MAC are non-motile, facultative intracellular bacteria which means they can survive both inside and outside the cell.
They’re also aerobic which means they need oxygen to survive.
They have a high content of mycolic acid in their cell wall, which makes them waxy, hydrophobic and impermeable to routine stain such as Gram stain.
So, they need special staining methods to be visualized such as Ziehl-Neelsen staining which is able to penetrate the waxy mycobacterial cell wall.
So, the stain binds to the mycolic acid in the mycobacterial cell wall and after staining, an acidic decolorizing solution is applied which removes the red dye from the background cells, tissue fibres, and any organisms in the smear except Mycobacteria, which retain the dye; and this is why they are called “acid-fast,” and they appear bright red on a blue background.
Finally, MAC are slow growing bacteria, and it typically takes them 10 to 21 days to grow on a medium called Lowenstein Jensen.
MAC are ubiquitous in soil and water and they are thought to enter the body through inhalation.
Once inside the body, they adhere to mucosal epithelial cells in the respiratory tract, and infect the macrophages that try to destroy them.
Macrophages try to break down the MAC organisms inside an intracellular organelle called a lysosome, which contain digestive enzymes.
However, MAC has unique, antigenic lipids called glycopeptidolipids, or GLPs, which are found on the surface of the cell.
These GLPs act as a protective barrier against lysosomal enzymes, allowing the bacteria to survive and multiply inside macrophages.
When these mycobacteria multiply they can cause inflammation, and this attracts more macrophages to the area.
They try to quarantine the invaders by forming granulomas, and as these grow bigger, they form nodules.
Eventually, this leads to nodular bronchiectasis and the inflammation causes damage to the bronchi, which become scarred and dilated.
The damaged bronchi have diminished mucociliary activity as well as decreased local immune function, and thereby lose their ability to move foreign material out of the lungs, so mucus can collect in these dilated areas making it the perfect environment for bacterial growth.
Nodular bronchiectasis tends to develop slowly, but in some cases the more aggressive and severe fibrocavitary disease occurs.
Here the mycobacteria invades the lung tissue, causing damage, severe fibrosis, and formation of cavities, much like tuberculosis.
Since MAC are aerobic organisms, these cavities tend to be in the air-rich upper lobes of the lungs.
In rare cases, and almost universally in individuals with compromised immune systems, the infected macrophages can move into the lymphatics and spread the bacteria to other parts of the body, especially to the spleen, liver and bone marrow.
And from these organs, they can spread to the bloodstream, causing disseminated disease.
Now, MAC usually cause chronic lung infection in people who already have an underlying lung disease, such as chronic obstructive pulmonary disease, cystic fibrosis or bronchiectasis.